Schmid, Evelyn ; Neef, Stefan ; Berlin, Christopher ; Tomasovic, Angela ; Kahlert, Katrin ; Nordbeck, Peter 
; Deiss, Katharina ; Denzinger, Sabrina ; Herrmann, Sebastian ; Wettwer, Erich ; Weidendorfer, Markus ; Becker, Daniel ; Schäfer, Florian ; Wagner, Nicole ; Ergün, Süleyman ; Schmitt, Joachim P ; Katus, Hugo A ; Weidemann, Frank ; Ravens, Ursula ; Maack, Christoph ; Hein, Lutz ; Ertl, Georg ; Müller, Oliver J ; Maier, Lars S ; Lohse, Martin J ; Lorenz, Kristina
; Deiss, Katharina ; Denzinger, Sabrina ; Herrmann, Sebastian ; Wettwer, Erich ; Weidendorfer, Markus ; Becker, Daniel ; Schäfer, Florian ; Wagner, Nicole ; Ergün, Süleyman ; Schmitt, Joachim P ; Katus, Hugo A ; Weidemann, Frank ; Ravens, Ursula ; Maack, Christoph ; Hein, Lutz ; Ertl, Georg ; Müller, Oliver J ; Maier, Lars S ; Lohse, Martin J ; Lorenz, Kristina 
Zusammenfassung
In heart failure therapy, it is generally assumed that attempts to produce a long-term increase in cardiac contractile force are almost always accompanied by structural and functional damage. Here we show that modest overexpression of the Raf kinase inhibitor protein (RKIP), encoded by Pebp1 in mice, produces a well-tolerated, persistent increase in cardiac contractility that is mediated by the ...
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